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A549 Lung cancer Cells - DOAJ

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Last Updated: 23 April 2022

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Synthesis of Novel Conjugated Linoleic Acid (CLA)-Coated Superparamagnetic Iron Oxide Nanoparticles (SPIONs) for the Delivery of Paclitaxel with Enhanced In Vitro Anti-Proliferative Activity on A549 Lung Cancer Cells

Non-Small Cell Lung Carcinoma: The use of Superparamagnetic Iron Oxide Nanoparticles as a nanomedicine can result in the delivery of anticancer drugs with minimal side effects. With the CLA-coated PTX-SPIONs against a lung adenocarcinoma cell line after 72 h, with a reported cell viability of 17. 1%. The CLA-coated PTX-SPIONs exhibited enhanced inhibition of A549 cell proliferation in comparison to pristine PTX, indicating that the nanomedicine could be used as a more convenient therapeutic device in NSCLC therapy.

Source link: https://doi.org/10.3390/pharmaceutics14040829


Formulation Design, Statistical Optimization, and In Vitro Evaluation of a Naringenin Nanoemulsion to Enhance Apoptotic Activity in A549 Lung Cancer Cells

Optimized NAR-NE was tested in A549 lung cancer cells using cell viability, flow-cytometric assays, and enzyme-linked immunosorbent assays. The nanoemulsion exhibited excellent thermodynamic and physical stability against phase separation and storage, with an initial burst leak followed by a controlled and monitored release for a longer period of 24 hours. In A549 lung cancer cells, concentration-dependent cytotoxicity was greater than that of free NAR. At the G2/M and cell cycle arrest phase induced by NAR-NE, the percentage of apoptotic cells and cell cycle arrest was significantly higher than those produced by free NAR. NAR-NEs were more effective than the NAR in lowering Bcl2 expression, while increasing pro-apoptotic Bax and caspase-3 production. In addition, stabled NAR-NE may be a good drug delivery system to increase the effects of NAR in lung cancer treatment.

Source link: https://doi.org/10.3390/ph13070152


Overexpression of the lung cancer-prognostic miR-146b microRNAs has a minimal and negative effect on the malignant phenotype of A549 lung cancer cells.

INTRODUCTION: MiR-146b-5p and -3p microRNAs in human non-small cell lung cancer cells are linked to recurrence of the disease following surgery. In A549 human lung cancer cells, the effect of miR-146b overexpression was investigated to clarify this. In an early stage NSCLC with recurrence, the association of miR-146b-5p and -3p expression as well as a recurrence was analyzed. PRINCIPAL FINDINGS: A549 pre-miR-146b microRNAs had 3-8-fold higher amounts of both miR-146b microRNAs and control cells than control cells, according to reports. Both miR-146b microRNAs were 7-10fold higher in stroma than in cancerous epithelia, and high miR-146b-5p levels were predictive of recurrence in human NSCLC tumors. MiR-146b's prognostic value of the two microRNAs could be because of miR-146b-5p and -3p overexpression, not cancerous epithelia of tumors, as shown by the conflicting recurrence-predictive values of the two microRNAs, or because miR-146b expression changes in non-cancerous stroma and not tumor epithelia of tumors.

Source link: https://doi.org/10.1371/journal.pone.0022379


Middle infrared radiation induces G2/M cell cycle arrest in A549 lung cancer cells.

While there are studies looking at the effects of broadband infrared radiation on cancer cells, the effects of middle-infrared radiation are still unclear. To irradiate A549 lung adenocarcinoma cells, a MIR emitter with a wavelength band in the 3-5 m region was used in this study. Because MIR treatment led to DNA double-strand break marker -H2AX and sensor 53BP1, it means the MIR-induced cell cycle arrest resulted from DSB. This article discusses the possibility of MIR in lung cancer therapy by inciting DSB and blocking cell cycle progression.

Source link: https://doi.org/10.1371/journal.pone.0054117


Anti-cancer activity of biosynthesized silver nanoparticles using Avicennia marina against A549 lung cancer cells through ROS/mitochondrial damages

By MTT assay, the anti-cancer property of synthesized Ag NPs was reported at 50 g/mL against A549 lung cancer cells. At least, the test revealed that the synthesized Ag NPs had enhanced anti-cancer activity against A549 cells at lowest concentrations.

Source link: https://doi.org/10.1016/j.sjbs.2020.08.029


Cisplatin-loaded superparamagnetic nanoparticles modified with PCL-PEG copolymers as a treatment of A549 lung cancer cells

The main aim of the present paper is to demonstrate a new method for the chemically and chemically altering of Fe3O4 superparamagnetic nanoparticles by physical and chemical retention. In a lung cancer cell line, these modified nanoparticles were used to encapsulate cisplatin as an anticancer drug, and the effect of nanocapsulated cisplatin has been investigated. Cisplatin nanoparticles coated with Cisplatin are ready to use with the copolymer containing iron superparamagnetic nanoparticles, the amount of medicine, size, and surface morphology have been tested for medicine entrapment success, as well as surface morphology and entrapment sensitivity. The findings of the research showed that nanocapsulated cisplatin had a significant cytotoxic and anticancer effect in vitro of the lung cancer cell line in vitro, and it can be concluded that this approach has the ability to satisfaction with some of the main chemotherapy constraints and may be a promising option for future lung cancer therapy programs.

Source link: https://doi.org/10.22034/nmrj.2019.04.002


COPD promotes migration of A549 lung cancer cells: the role of chemokine CCL21

We investigated whether COPD can be associated with increased migration of non-small-cell lung cancer cells A549, and, if so, whether this reaction may be attributed to the changes in manufacturing and activity of chemokines CCL21, CXCL5, and CXCL12. The migration of A549 cells by the polycarbonate membrane and basement membrane extract into a chemotactic gradient elicited by serum from patients with COPD was significantly higher than that of healthy donors, according to the study. CCL21 and CXCL12, but not CXCL5, were also present in serum from patients with COPD. CCL21 was the sole source of CCL21-mediated cancer cell transplantation following serum therapy with serum from patients with COPD, which was exclusively controlled by CCL21 and CXCL12-dependent signaling. Our findings show that COPD can influence lung cancer progression by CCL21-dependent boosts of cancer cell migration.

Source link: https://doaj.org/article/10e27af787b04a5d86463892e936135a


Inhibition of mPGES-1 or COX-2 Results in Different Proteomic and Lipidomic Profiles in A549 Lung Cancer Cells

In experimental models of cancer and inflammation, pharmacological inhibition of microsomal prostaglandin E synthase -1 for selective reduction of prostaglandin E2 biosynthesis is helpful. We compared the effects of mPGES-1 inhibitor Compound III with cyclooxygenase -2 inhibitor NS-398 on protein and lipid profiles in interleukin -1-induced lung cancer cells using mass spectrometry herein. PGE2 production and increased PGF2 and thromboxane B2 production slowed, while COX-2 inhibition reduced the production of all three prostanoids. In addition, pathway studies indicated that CIII brought cell death of cancer cells to a higher rate, while NS-398 reduced the same function. Our results reveal changes in protein and lipid profiles after inhibition of mPGES-1 or COX-2, which has important implications on the therapeutic efficacy of mPGES-1 inhibitors as adjuvant therapy in cancer.

Source link: https://doi.org/10.3389/fphar.2019.00636


Hinokitiol Inhibits Migration of A549 Lung Cancer Cells via Suppression of MMPs and Induction of Antioxidant Enzymes and Apoptosis

Hinokitiol, a natural monoterpenoid from Calocedrus formosana's heartwood, has been shown to have anticancerant properties against a number of cancer cell lines, according to several cancer cell lines. However, the complete molecular mechanisms and the inhibiting roles of hinokitiol on adenocarcinoma A549 cells have yet to be fully understood. Human lung adenocarcinoma A549 cells in vitro were migrated by occipation. Hence, the new research was designed to assess the effects of hinokitiol on human lung adenocarcinoma A549 cells in vitro. Hinokitiol dramatically reduced the expression of matrix metalloproteinases -2/-9 in A549 cells, resulting in an increase in protein expression of matrix metalloproteinases -2/-9. Remarkably, when A549 cells were exposed to hinokitiol, there was an increase in the activities of antioxidant enzymes catalase and superoxide dismutase from cell degradation, which was remarkable. The findings reveal a new therapeutic role for hinokitiol in lung cancer chemoprevention.

Source link: https://doi.org/10.3390/ijms19040939


Maslinic Acid Induces Mitochondrial Apoptosis and Suppresses HIF-1α Expression in A549 Lung Cancer Cells under Normoxic and Hypoxic Conditions

A549 cells were analyzed under normoxic and hypoxic conditions, and the apoptotic effects of maslinic acid were determined by apoptotic mechanism. This agent, who was 4–64 mol/L, reduced Na+-ATPase production and increased caspase-3 expression under normoxic conditions, but it caused these changes under hypoxic conditions at 8–64 %. HIF-1, VEGF, survivin, and iNOS were all ineffective in cell pre-treatment with YC-1, an HIF-1 inhibitor, and iNOS. Under both conditions, reactive oxygen species and nitric oxide levels in MA at 8-64 and 32-64 decreased.

Source link: https://doi.org/10.3390/molecules191219892

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions